The human gut is inhabited by diverse microorganisms that play crucial roles in health and disease. Gut microbiota dysbiosis is increasingly considered as a vital factor in the etiopathogenesis of irritable bowel syndrome (IBS), which is a common functional gastrointestinal disorder with a high incidence all over the world. However, investigations to date are primarily directed to the bacterial community, and the gut mycobiome, another fundamental part of gut ecosystem, has been underestimated. Intestinal fungi have important effects on maintaining gut homeostasis just as bacterial species. In the present article, we reviewed the potential roles of gut mycobiome in the pathogenesis of IBS and the connections between the fungi and existing mechanisms such as chronic low-grade inflammation, visceral hypersensitivity, and brain-gut interactions. Moreover, possible strategies targeted at the gut mycobiome for managing IBS were also described. This review provides a basis for considering the role of the mycobiome in IBS and offers novel treatment strategies for IBS patients; moreover, it adds new dimensions to researches on microorganism.

Accumulating evidence from studies in humans and animal models has elucidated that gut microbiota, acting as a complex ecosystem, contributes critically to colorectal cancer (CRC). The potential mechanisms often reported emphasize the vital role of carcinogenic activities of specific pathogens, but in fact, a series of metabolites produced from exogenous dietary substrates or endogenous host compounds occupy a decisive position similarly. Detrimental gut microbiota-derived metabolites such as trimethylamine-N-oxide, secondary bile acids, hydrogen sulfide and N-nitroso compounds could reconstruct the ecological composition and metabolic activity of intestinal microorganisms and formulate a microenvironment that opens susceptibility to carcinogenic stimuli. They are implicated in the occurrence, progression and metastasis of CRC through different mechanisms, including inducing inflammation and DNA damage, activating tumorigenic signaling pathways and regulating tumor immunity. In this review, we mainly summarized the intimate relationship between detrimental gut microbiota-derived metabolites and CRC, and updated the current knowledge about detrimental metabolites in CRC pathogenesis. Then, multiple interventions targeting these metabolites for CRC management were critically reviewed, including diet modulation, probiotics/prebiotics, fecal microbiota transplantation, as well as more precise measures such as engineered bacteria, phage therapy and chemopreventive drugs. A better understanding of the interplay between detrimental microbial metabolites and CRC would hold great promise against CRC.

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Contract grant sponsorNational Natural Science Foundation of China; Contract grant number: 81260214.BackgroundRecent studies have highlighted the diagnostic value of Gadolinium‐ethoxybenzyl‐diethylenetriamine pentaacetic acid (Gd‐EOB‐DTPA)‐enhanced MRI in small hepatocellular carcinoma (HCC). Ki67 and CD34 are histologic markers that reflect the proliferation of tumor cells and the microvascular density (MVD).PurposeTo explore the diagnostic value of Gd‐EOB‐DTPA‐enhanced MRI for Ki67 expression and MVD in HCC.Study TypeRetrospective.SubjectsIn all, 180 patients with HCC.Field Strength/Sequence3.0T, Gd‐EOB‐DTPA‐enhanced T1WI volumetric interpolated breath‐hold examination (VIBE) axial fat suppression plain, and enhanced scanning.AssessmentThe T1 relaxation time (T1rt) and signal intensity (SI) of the lesion were measured. The Ki67 expressions and MVD were evaluated by immunohistochemistry.Statistical TestReceiver operating characteristic (ROC) curves were used to analyze the diagnostic efficacy of T1rt for high Ki67 expression (≥50%) and high MVD (≥100).ResultsThe T1rt‐20min, rrT1rt‐20min, and SI‐hepatobiliary phase (SI‐HBP) were strongly correlated with Ki67, the r values were 0.846, –0.765, and –0.760 (P < 0.05), respectively. There were moderate correlations with CD34, with r values –0.444, 0.336, and –0.463 (P < 0.05), respectively. The T1rt‐Pre, T1rt‐20min, SI‐Pre, and SI‐HBP were significantly different both between the high and low ki67 expression groups (P < 0.05) and between the high MVD and low MVD groups (P < 0.05). In the two groups the T1rt‐20min and SI‐HBP was 800.06 ± 128.91 vs. 530.06 ± 139.29 (P < 0.05) and 122.29 ± 39.39 vs. 173.49 ± 46.15 (P < 0.05); T1rt‐20min was found to have high diagnostic efficiency for high ki67 expression (area under the curve [AUC], 0.937; P < 0.05) T1rt‐20min had moderate diagnostic value for high MVD (AUC, 0.716; P < 0.05).Data ConclusionThe T1rt and SI of Gd‐EOB‐DTPA‐enhanced MRI were correlated with Ki67 expression and MVD. T1rt‐20min has a high diagnostic value for high ki67 expression and high MVD in HCC tissues.Level of Evidence: 3Technical Efficacy Stage: 2J. Magn. Reson. Imaging 2020;51:1755–1763.